Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a specific citrate lyase method, renal excretion of citrate was studied in 32 normal Chinese males, 30 nondialysed uremic male patients and 35 male subjects who had a history of nephrolithiasis. Patients with uremia or nephrolithiasis were found to have a lower urinary citrate excretion. Tubular reabsorption of citrate was markedly decreased in uremic patients, but in stone patients, the increased renal tubular reabsorption of citrate was only found in patients with hypocitraturia, whose renal citrate excretion was below 650 mumol/day and whose urinary magnesium was also low. Hypocitraturia was found in 45% (16/35) of the patients with renal stones whether their filtered load of citrate was normal or subnormal. Urinary citrate excretion was correlated with renal creatinine clearance in both normal subjects and in patients with renal stones or chronic renal failure. However, urinary phosphate correlating with urinary citrate was only found in normal subjects and in patients with kidney stones. In normal subjects, we found a positive correlation between urinary citrate and phosphate, but in stone patients, we found a negative correlation. Hypercalciuria and hyperoxalaturia were noted in some stone formers, who had, moreover, a lower urinary citrate and ascorbate excretion level. Mean urinary ascorbate excretion in patients with renal stones was markedly below that in normal subjects. Thus, we suggest that low urinary citrate excretion may be prevalent in patients with renal stones or chronic renal failure, and that hypocitraturia can be found in some stone formers, whose tubular reabsorption of citrate may be increased.
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PMID:Renal excretion of citrate in patients with chronic renal failure or nephrolithiasis. 167 8

Renal calcifications have been described in very low birth weight (VLBW) infants, and diuretic drug-associated hypercalciuria is believed to play a role in the pathogenesis of this lesion. Hyperoxaluria is an important cause of renal stone formation in children and adults. Because parenteral nutrition solutions contain the oxalate precursors ascorbate and glycine, the relationship between total parenteral nutrition administration and oxalate excretion in VLBW infants was examined. Administration of approximately 0.5 g of total parenteral nutrition protein per kilogram per day to VLBW infants was associated with an increased urinary oxalate concentration and an increased urinary oxalate to creatinine ratio, when compared with VLBW infants receiving a glucose and electrolyte solution. A further increase in urinary oxalate concentration and oxalate to creatinine ratio was noted when total parenteral nutrition protein was increased to approximately 1.5 g of protein per kilogram per day. In VLBW infants who receive total parenteral nutrition, elevated urinary oxalate concentrations may develop and may be a factor in the pathogenesis of nephrocalcinosis in these infants.
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PMID:Urinary oxalate excretion by very low birth weight infants receiving parenteral nutrition. 250 54

Laboratory animal, clinical and epidemiological studies in the published literature have been reviewed in order to establish whether excessive salt intake is an important risk factor for the development of osteoporosis and whether an intervention strategy based on salt restriction would be beneficial in the prevention of osteoporosis. Genetic factors appear to be far more important than the combination of nutritional, hormonal, environmental and lifestyle factors in the pathogenesis of osteoporosis. The most important single non-genetic factor is oestrogen deficiency in postmenopausal women. Preventive measures should be aimed at maximizing peak bone mass at skeletal maturity and retarding bone loss thereafter. Apart from postmenopausal oestrogen deficiency, various factors have been incriminated as risk factors for osteoporosis, and these include age at menarche, age at and years since menopause, insufficient physical exercise, alcohol, smoking, low calcium intake, low or high protein intake and high intake of phosphorus, sodium or caffeine. Many of the risk factors are considered to be weak, although when combined they could impact significantly on bone health. Increased intakes of various nutritional factors (potassium, magnesium, zinc, vitamin C), fibre and alkaline-producing fruit and vegetables favour adult bone health. Calcium homeostasis is normally well regulated such that increased calcium loss via the urine leads to increased calcium absorption from the gut. However, the duration of this adaptive process may be greater than that of many of the studies demonstrating that increased salt intake leads to both increased sodium and calcium in the urine. In any case, higher urinary calcium output appears to be seen only in a minority of humans in response to increased salt intake. As numerous factors-genetic, nutritional, hormonal and lifestyle-are involved in the maintenance of calcium homeostasis, it is difficult to devise human studies which adequately take into account all the important factors. Another difficulty is that many past studies have relied on imprecise methods for the measurement of bone resorption. Nor have studies based on the use of the laboratory rat produced clear answers to the problem because the rat, as a species, is uniquely deficient in its ability to handle the relevant minerals. Limited studies to date indicate that increased sodium intake neither exerts a consistent effect on various biomarkers of bone health nor leads to irreversible changes in the bone modelling process in men or in pre- or postmenopausal women. We conclude from the available evidence that increased sodium (or salt) intake is not an important risk factor for osteoporosis and that a reduction of salt intake from 9 to 6g/day in the diet would not be beneficial as an intervention measure in the prevention of osteoporosis. More research is needed to (i) assess the effects (especially long-term) of various nutrients including sodium on bone health, (ii) assess the long-term value of any intervention strategy involving reduced intake of a particular nutrient such as sodium; and (iii) determine whether subpopulations exist particularly in the elderly (e.g. sodium-responsive subjects) in which adaptation to sodium-induced hypercalciuria may be compromised. General prudence dictates that excessively high levels of dietary salt should be eschewed by those persons with raised blood pressure or a limited range of genetic disorders. However, for the generally healthy person there is no sound evidence that the consumption of salt at the present average level of 9g/day constitutes a risk factor for osteoporosis.
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PMID:Review of risk factors for osteoporosis with particular reference to a possible aetiological role of dietary salt. 1071 63

The prevalence of idiopathic nephrolithiasis is increasing in rich countries. Dietary manipulation could contribute to the prevention of both its first appearance and the recurrence of the disease. The target of dietary treatment is to decrease the "urinary lithogenic risk factors" such as low urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, hyperphosphaturia, hypocitraturia, hypomagnesuria and excessively alkaline or acid urinary pH. Due to the lack of randomized controlled trials focused on this problem, there is not ample evidence to confidently recommend dietary changes. Despite this, numerous recent and past experiences support modification of diet as having a primary role in the prevention of nephrolithiasis. In particular, it is recommended to limit animal protein and salt intake, to consume milk and derivatives in amounts corresponding to calcium intake of about 1200 mg/day and to assume fiber (40 g/day), vegetables and fruit daily avoiding foods with high oxalate content. Furthermore, vitamin C intake not exceeding 1500 mg/day plays a protective role as well as avoiding vitamin B6 deficiency and abstaining, if possible, from vitamin D supplements. Lastly, it is recommended to drink enough water to bring the urinary volume up to at least 2 L/day and, as much as possible, to use fresh or frozen products rather than prepacked or precooked foods which are often too rich in sodium chloride.
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PMID:Dietary treatment of nephrolithiasis. 2246 Sep 96